Fetal striatal transplants reinstate the electrophysiological response of pallidal neurons to systemic apomorphine challenge in rats with excitotoxicstriatal lesions

Previous studies with single-unit recording and 2-[C-14]deoxyglucose quanti tative autoradiography have shown that systemic administration of apomorphi ne increases the functional activity of pallidal neurons, and that the enha ncement in the globus pallidus (GP) activity is abolished by striatal lesio ns. The present study employing electrophysiological techniques tested whet her embryonic striatal tissue implanted in the excitotoxically damaged stri atum of rats may affect the lesion-induced alteration in the neuronal respo nse of GP to apomorphine. Systemically administered apomorphine significant ly increased spontaneously firing rates of GP cells. The blockade of dopami ne receptors with haloperidol reversed the increased rate to baseline level s. Quinolinate-induced striatal lesions attenuated the rate-increasing effe ct of apomorphine. Embryonic striatal grafts placed in the lesioned striatu m restored the response of GP cells to systemic apomorphine. The graft-medi ated restoration of the GP neuron response to apomorphine were accompanied by an improvement in the motor asymmetry induced by this drug. Considering previous anatomical data to demonstrate extensive innervation of the GP by embryonic striatal grafts, the present results suggest that the grafts reco nstruct the functional striatopallidal pathway which is capable of transmit ting apomorphine-induced changes in the neuronal activity.